Abstract
DNA mutations are inevitable. Despite proficient DNA repair mechanisms, somatic cells accumulate mutations during development and aging, generating cells with different genotypes within the same individual, a phenomenon known as somatic mosaicism. While the existence of somatic mosaicism has long been recognized, in the last five years, advances in sequencing have provided unprecedented resolution to characterize the extent and nature of somatic genetic variation. Collectively, these new studies are revealing a previously uncharacterized aging phenotype: the accumulation of clones with cancer driver mutations. Here, we summarize the most recent findings, which converge in the novel notion that cancer-associated mutations are prevalent in normal tissue and accumulate with aging.
Highlights
OPEN ACCESSCase Western Reserve University School of Medicine, UNITED STATES
DNA encodes the basic instructions to construct an organism during its development, and its stability is essential to life
We propose aberrant clonal expansion (ACE) to be a previously underappreciated aging phenotype that is universal in most organisms, affects multiple tissues, and likely helps explain why aging is the biggest risk factor for cancer
Summary
Case Western Reserve University School of Medicine, UNITED STATES. The funders had no role in the preparation of the article
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